ArticleShock (Augusta, Ga.)2021
Tender Coconut Water Protects Mice From Ischemia-Reperfusion-Mediated Liver Injury and Secondary Lung Injury.
Article in Shock (Augusta, Ga.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Inter-Organ Communication in Pulmonary Fibrosis: Systemic Modifiers of a Lung-Centered Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Anticancer Properties Against Select Cancer Cell Lines and Metabolomics Analysis of Tender Coconut Water.Anti-cancer agents in medicinal chemistry · 2025Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
abstractOrgan injury by oxidative and inflammatory mediators occurs during ischemia-reperfusion (I/R) of the liver. Remote organ injury secondary to liver I/R increases the systemic insult. Tender coconut water (TCW) has been studied in chemical and fructose-induced liver injury but its ability to decrease tissue injury in clinically relevant injury models is unknown. We evaluated the therapeutic potential of TCW in preventing liver I/R injury and associated remote organ injury. Mice were fed sugar water (SUG; control) or TCW for a week and then subjected to 60 min of liver ischemia followed by reperfusion for 6 h. Plasma alanine transaminase levels, tissue damage, and mRNA levels of Nos2, Tnf, and Il6 were significantly lower in mice fed TCW prior to I/R. Plasma cytokines followed liver cytokine patterns. TCW increased mRNA levels of the anti-oxidant genes Hmox1 and Ptgs2 in the liver of mice subjected to I/R. Remote lung injury from liver I/R was also decreased by TCW feeding as evident by less neutrophil infiltration, decreased pro-inflammatory Il6, and increased anti-inflammatory Il10 mRNA levels in the lung. To examine macrophage activation as a potential mechanism, TCW pretreatment decreased the amount of nitrite produced by RAW264.7 macrophages stimulated with LPS. The levels of Nos2, Il1b, Tnf, and Il6 were decreased while Il10 and Hmox1 mRNA levels were significantly up-regulated upon LPS stimulation of TCW pretreated RAW264.7 macrophages. Collectively, our results indicate that TCW decreased hepatic I/R-mediated damage to liver and lung and suggest that decreased macrophage activation contributes to this effect.
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Registered trials
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